The prupose of this research is to determine whether the central cardiovascular effects of angiotensin II in the brainstem require the participation of an endogenous brain opiate system. It is our hypothesis that activation of peptidergic neurons facilitates the expression of centrally mediated cardiovascular pressor responses to angiotensin II by either a direct effect on bulbar sympathetic pressor pathways or by inhibition of central baroreceptor activity. These experiments are designed to: 1) determine if the endogenous opiate system modulates the central action of angiotensin II in conscious dogs; 2) compare the chemical (angiotensin II) versus electrical stimulation of the area postrema; 3) elucidate the mechanisms of the opiate-angiotensin II interaction at the level of the brainstem through microinjection techniques to determine participation of other neurotransmitters; 4) investigate the opiate-baroreceptor interrelationship; 5) characterize the influence of the opiate system in conditions where endogenous levels of angiotensin II are altered (altered sodium states, renal hypertension). Acquisition of knowledge from this study can lead to a better understanding of disease states associated with altered levels of endogenous angiotensin II. It is also possible that knowledge of the interplay between neurotransmitters and neuropeptides (angiotensin II enkephalin) could shed light upon the general way by which neurons possessing tonic cardiovascular activity are affected by locally released peptides.